We hypothesize that because of cocaine's effect on the developing catecholamine system, prenatal cocaine exposure should interfere with the infant's ability to regulate and control arousal, thereby affecting the normal development of attention grocesses. Thus, neonates and young infants of cocaine abusing mothers will differ in how they integrate arousal and attention as compared to (a) non-exposed, drug-free controls, and (b) infants with other CNS risk conditions. Furthermore, these differences will persist through the first year of life and be detected primarily using tasks that require visual information processing. Preliminary evidence indicates that cocaine-exposed infants tend to look at more stimulating events regardless of manipulations of arousal that would normally shift preferences to less stimulating events. This behavioral difference is in marked contrast to that of infants with structural CNS insults and to that of normal infants. Specifically, we propose: (a) to replicate and extend these studies during the neonatal period; (b) to study the interaction of early cocaine-exposure with developmental changes in attentional and perceptual systems and with subsequent development of recognition memory, predicting that cocaine exposure will interfere with the normal development of these processes when evaluated at 1, 4, and 7 months postterm age; and (c) determine the degree to which cognitive development at 10 and 13 months posterm age, measured by mastery motivation and response to surprising experiences, is affected cocaine exposure, predicting that cocaine exposure will affect the development of motivational systems and will alter attention to unusual information in the environment, resulting in the need for longer familiarization to appreciate violations of expectancies or possible from impossible events. In addition, we expect to find corroborative evidence of the adverse effect of in utero cocaine exposure by studying neonatal neurobehavioral performance, salivary cortisol responses as an indicator of reaction to stress, brainstem auditory evoked responses as an indicator of development of neural transmission speed in relation to IUGR produced by in utero stress, and heart-rate variability changes as an indicator of altered ANS integration with environmental experiences.